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Antagonist Protocol Estrogen Priming ???

Anyone know if these are very different protocols??

My nurse told me that when I meet with the doc next week, we will discuss Antagonist Protocol for a third IVF. (I have been a poor responder in 1st IVF and a non-responder in Microdose Flare Protocol. Had 2 cycles within 21/2 months. I had zero response to second IVF.)

I have read that Estrogen Priming is seen to have good responses for poor responders like myself. I have read the Antagonist Protocol information that was posted at this site.

Are Antagonist and Estrogen Priming the same?

If anything, does anyone have personal experience with these protocols?

Bluejeans - they are not the same but they go together for poor responders. The E2 priming is for down regulation before the stim cycle and adds two to three IM E2V shots during the stim cycle. The antagonist protocol is for stims and it involves using ganilrex or cetrotide with high stims of follistim. I am using this protocol this cycle and I am currently in the E2 priming protocol and start stims next week. Many of the women on our weekly board have switched to antagonist cycles and they are much better producers. Somewhere on this board is an entire article on this also. Let me see if I can find it.

Estrogen priming protocols: Older women (over 40 yrs), women who have demonstrated a prior reduced ovarian response to COH and those who by way of significantly raised cycle day 3 FSH and reduced Inhibin B levels are considered likely to be “poor responders”, are first given GnRH agonist for a number of days to effect pituitary down-regulation. Upon menstruation and confirmation by ultrasound blood estradiol measurement that adequate ovarian suppression has been achieved, the dosage of GnRH agonist is drastically lowered (or the agonist is replaced with a GnRH antagonist) and the woman is givens twice-weekly injections of estradiol for a period of 7-10 days. COH is then initiated using a relatively high dosage of FSH-dominant gonadotropins such as Folistim or Gonal F that is continued along with daily administration of GnRH agonist/antagonist until the “hCG trigger”. A recently completed study has demonstrated the efficacy of this protocol and the ability to significantly improve ovarian response to gonadotropins in many of hitherto “resistant patients

The GnRH Agonist/Antagonist Conversion Protocol (A/ACP) : It is our position that some form of pituitary blockade, either in the form of a GnRH agonist (e.g. Lupron, Buserelin, Nafarelin, and Synarel. Decapeptyl) or a GnRH antagonist (e.g. Antagon, Cetrotide, Cetrorelix, and Ganarelix) is an essential component in ovarian stimulation of “poor responders” undergoing IVF. If this is not done, a progressive rise in LH –induced ovarian androgens (male hormones ….mainly testosterone) will inevitably affect follicle/ egg development, resulting in compromised embryo quality.
The follicles/ eggs of women on GnRH-agonist “flare protocols” are exposed to an exaggerated Lupron-induced LH release, (the “flare effect” while the follicles/eggs of women, who receive GnRH antagonists starting 6-8 days into the stimulation cycle are exposed to endogenous LH -induced ovarian androgens( especially testosterone). This might not be problematic in “normal responders” but could be decidedly prejudicial in “poor responders” and older women where endogenous basal LH levels are often raised and the ovaries may be inordinately sensitive to LH and where excessive exposure of follicles and eggs to testosterone could severely compromise egg development and thus embryo quality.
exhausted of its LH and residual minimal LH is present in the circulation by the time stimulation with gonadotropins begins, the above mentioned adverse testosterone-effect is largely negated. On the down side is the fact that prolonged administration of GnRH agonists such as Lupron (such as with the GnRH agonist down-regulation protocol could suppress subsequent ovarian response to ovarian stimulation with gonadotropins, by competitively binding with ovarian FSH receptors. We introduced of our Agonist/Antagonist Conversion Protocol (A/ACP) more than a year ago in an effort to counter this effect.
With the A/ACP, low dose Antagon/Cetrotide is commenced at the onset of spontaneous menstruation or following bleeding that follows initiation of GnRH agonist (e.g. Lupron) therapy using a long-down-regulation protocol arrangement. We currently prescribe the A/ACP to most of our IVF patients regardless of whether they are “normal responders” or “poor responders”. Preliminary results suggest a significant improvement in egg number, egg/embryo quality as well as in implantation and viable IVF pregnancy rates. The A/ACP has however, proven to be most advantageous in “poor responders” where additional enhancement of ovarian response to gonadotropins may be achieved through incorporation of “estrogen priming”. We have reported on the fact that the addition of estradiol for about a week following the initiation of the A/ACP, prior to commencing FSH-dominant gonadotropin stimulation appears to further enhance ovarian response, presumably by up-regulating ovarian FSH-receptors.
There is one potential draw back to the use of the A/ACP, in that the sustained use of a GnRH antagonist ( e.g. Antagon/Cetrotide) throughout the stimulation phase of the cycle, appears to compromise the predictive value of serial plasma estradiol measurements as a measure of follicle growth and development in that the estradiol levels tend to be much lower in comparison to cases where agonist (Lupron) alone is used or where a “ conventional” GnRH antagonist protocol is employed ( i.e. antagonist administration is commenced 6-8 days following initiation of gonadotropin stimulation). Rather than being due to reduced production of estradiol by the ovary(ies), the lower blood concentration of estradiol seen with prolonged exposure to GnRH-antagonist, could be the result of a subtle, agonist-induced alteration in the configuration of the estradiol molecule , such that currently available commercial kits used to measure estradiol levels are rendered much less sensitive/specific. Thus when the A/ACP is employed, we rely much more heavily on ultrasound growth of follicles along with observation of the trend in the rise of estradiol levels, than on absolute estradiol values. Thus we commonly refrain from prescribing the A/ACP in “high responders” who are predisposed to the development of severe ovarian hyperstimulation syndrome (OHSS) and accordingly where the accurate measurement of plasma estradiol plays a very important role in the safe management of their stimulation cycles.
It is remarkable, that while using the A/ACP + "estrogen priming " in “poor responders “ whose FSH levels were often well above threshold limits, the cycle cancellation has consistently been maintained below 10% ( i.e. much lower than expected). Many of these patients who had previously been told that they should give up on using their own eggs, and switch to ovum donation because of “poor ovarian reserve”, have subsequently achieved viable pregnancies at SIRM using the A/ACP with “estrogen priming”.

Another Question

Why do the docs not put us on an Antagonist Protocol after a first poor response to IVF?

I was put on a Microdose Flare Protocol for my 2nd IVF. I did not respond at all.

However, a cyst was present in the u/s at the very beginning of IVF #2-docs still said to continue. 2nd IVF was also started within a month of the 1st IVF, which was cancelled with only three maturing follicles. I think my ovaries were pissed off at me.

Nic - Thank you for the information - I am planning on printing it out to try and digest it a little further. This is quite a bit different from my current IVF cycle. I was on Bravelle & Menopur until I had a follie at 14, then I was but on Ganarelix. Is this a common type of protocol for poor responders? Another question I have is, if you E2 is fine, but you have a high FSH, is this protocol for me?

bluejean, I see Nic already found the info for you. I told you the ladies here are great I was on the Micro Dose Flare protocol twice, the first time I responded nicely the second time I did not respond at all and was cancelled. It seems the Lupron suppresses us to much. I think that is why the ladies are having better luck with Ganarelix or Antagon. You do not have to have Estrogen priming with the Antagonist protocol. I would print Nics post and take it into your RE, and see what they say.

WJ, I don't think most ladies that use the EPO have issues with E2 levels.

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